The role of airway macrophages in apoptotic cell clearance following acute and chronic lung inflammation

Grabiec, Aleksander M.; Hussell, Tracy

While in sterile inflammation recognition of apoptotic cells by the immune system typically results in suppression of the ongoing inflammatory response, the complexity of this process and its biological effects greatly increase in the context of microbial infections. First, some enveloped viruses use PtdSer receptors to promote their entry into the host cells and facilitate infection and immune evasion [115] . The interaction between PtdSer exposed on the surface of the viral envelope and members of the TAM and TIM receptor families expressed on the target cell enables proximity to specific entry receptors and enhances engulfment of the virus [116] (Fig. 1c) . The relevance of this process, called 'apoptotic mimicry', has recently been confirmed for a broad range of virions, including Ebola and dengue viruses [117, 118] . Thus far, however, little is known about potential roles of this entry mechanism in pulmonary viral infections. The observation that the kinetics of influenza H1N1 virus clearance was unaffected in Axldeficient mice indirectly indicates that Axl is not important for control of this infection [2] , though Axl-H1N1 interaction has not been formally tested. Similarly, although TIM1 promotes internalisation and replication of several enveloped viruses, TIM1-mediated entry does not lead to a productive infection by influenza H7N1 and severe acute respiratory syndrome (SARS) coronavirus [117] , arguing against an important role of apoptotic mimicry in viral lung diseases.